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Fetal Alcohol Syndrome

FETAL ALCOHOL SYNDROME (FAS) is the leading known cause of mental retardation

and birth defects in the world. Fetal alcohol syndrome is a pattern of physical, behavioral and

cognitive abnormalities seen in individuals exposed to alcohol in uterus. Because alcohol is a

known teratogen and the damage done to a fetus by alcohol exposure is permanent, public

education about the dangers of prenatal alcohol exposure has been extensive. Many of the

features of the fetal alcohol syndrome are secondary to the effect of alcohol on brain

development. These include microcephaly, short palpebral fissures, the long smooth philtrum

and thin vermilion of the upper lip, joint anomalies, altered palmar crease pattern, and mental

retardation. Animal studies as well as a limited amount of human data also show that

maternal genotype is a key player : Advances in the development of novel antioxidant

therapies as an approach for fetal alcohol syndrome prevention. Peptides NAPVSIPQ (NAP)

and SALLRSIPA (SAL), related to activity-dependent neuroprotective protein (ADNP),

prevent alcohol-induced damage in a mouse model of FAS. In a recent study, the thyroxin

reversed the deficit both in the level of their genes and their social behaviour, research is

going on how the prenatal thyroid hormone supplementation reverses the behavioural deficits

in the fetal alcohol spectrum disorder model. Another study used a priori approach to assess

molecular phenotype in the cranial neural folds (head fold) of early mouse embryos soon

after maternal alcohol treatment. FAS can be modulated pharmacologically with PK11195, a

potent ligand with specific binding to the mitochondrial peripheral-type benzodiazepine

receptor recognition site. PK11195 has been shown to protect early mouse embryos from eye

and brain defects induced with diverse teratogens and to protect adult tissues from some

inflammatory lesions. Microarray transcript profiling of the embryonic head fold at 3.0 hr

after alcohol exposure or PK11195 counter-exposure enabled prioritization of candidate

pathways that integrate the genomic response with genetic susceptibility of the system. These

findings are consistent with the growing view that developmental exposure to alcohol alters

common signalling pathways linking receptor activation to cytoskeletal reorganization. The

programmatic shift in cell motility and metabolic capacity further implies cell signals and

responses that are integrated by the mitochondrial recognition site for PK11195.

CONCLUSIONS: Until the advent of effective prevention measures, it will remain

necessary to seek ways to treat the life-long neurobehavioral consequences of prenatal

alcohol exposure. Nevertheless, alcohol is a widely accepted and legal social drug, and many

pregnant mothers continue to drink it while pregnant. Whereas, FAS is totally preventable by

avoiding alco

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Fetal Alcohol Syndrome

  1. 1. FETAL ALCOHOL SYNDROME BY SHAIK SHAHEENA VIGNAN’S UNIVERSITY VADLAMUDI
  2. 2. When a woman drinks alcohol during pregnancy, she risks giving birth to a child who will be born with fetal alcohol syndrome (FAS).
  3. 3. Alcohol travels through this path and affects the baby’s development, particularly the heart and the brain. PATHWAY OF ALCOHOL FROM MOTHER TO FETUS
  4. 4. AN ARTICLE QUOTES THAT ‘ INDIAN FEMALES ARE INCREASINGLY TURNING EXPERIMENTAL’ THEIR RISING ASPIRATIONS AND EXPOSURE TO DIFFERENT LIFESTYLES APPEARS TO BE DRIVING THIS DESIRE TO HAVE NEWER EXPERINCES AND THAT INCLUDES EXPERIMENTING WITH ALCOHOL
  5. 5. Excessive alcohol exposure can cause damage during all stages of prenatal development. • Pre-implantation: first 2 weeks • Embryonic: 3-8 weeks after conception • Fetal: from week 9 until birth
  6. 6. Alcohol can cause permanent damage to a baby before most women realize they are pregnant.
  7. 7. Fetal Alcohol Syndrome (FAS) which is characterized by 1. central nervous system problems 2. low birth weight and height 3. typical facial features ALCOHOL RELATED BIRTH DEFECTS
  8. 8. • attention deficits • language difficulties • learning disabilities • impulsive behavior • poor judgment CHILDREN WITH ALCOHOL RELATED BIRTH DEFECTS TYPICALLY HAVE:
  9. 9. FETAL ALCOHOL SYNDROMECLEFT LIP/PALATE FAILURE MIDLINE CLEAVAGE OF EMBRYONIC FOREBRAIN SINGULAR VENTRICULAR CAVITY
  10. 10. Similarities in mouse and human embryogenesis provide opportunities to study the effects of alcohol on development. 5 mm. Mouse (10 days old) Human (approx. 28 days old) EYE HEART UPPER LIMB (ARM) 3 mm.
  11. 11. CELLS THAT SHOULD FORM MIDLINE STRUCTURES OF THE BRAIN AND FACE ARE KILLED BY ALCOHOL Developing brain and face Heart Mouse embryo (viewed from the front) at a stage corresponding to a 22-23 day old human. A close-up view of an alcohol-exposed mouse embryo shows cells killed by alcohol that have taken up a dark blue stain.
  12. 12. EYE EYE A C B D MOUTH MOUTH NOSTRILS NOSTRILS MIDLINE STRUCTURES OF THE FACE AND BRAIN ARE DEFICIENT IN ALCOHOL-EXPOSED MOUSE EMBRYOS AND IN INDIVIDUALS WITH FAS THE FACE OF A CHILD WITH FULL-BLOWN FAS HAS FEATURES THAT CAN BE CAUSED BY DAMAGE TO MIDLINE STUCTURES. COMPARISON OF THE FACE (A) AND INTERIOR OF THE BRAIN (B) OF A NORMAL MOUSE EMBRYO AND ONE DAMAGED BY ALCOHOL (C&D) SHOWS THAT THE NOSTRILS ARE ABNORMALY POSITIONED (C) AND THE BRAIN IS MISSING MIDLINE STRUCTURES (D).
  13. 13. DIFFERENT APPROACHES FOR THE DIAGNOSIS TREATMENT PRVENTION OF ALCOHOL RELATED NEUROLOGICAL DISORDER ESPECIALLY FETAL ALCOHOL SYNDROME ARE DISCUSSED
  14. 14. • A variety of alcohol-induced alterations in maternal, placental and/or fetal physiology have been proposed as the basis for this retarded fetal growth. Using the embryonic chick as a model they have measured ethanol-induced growth suppression as a function of embryonic age and ethanol dosage. THE SUPPRESSION OF CELL DIVISION IS PROPORTIONAL TO THE ETHANOL DOSE. • Moreover, alcohol abuse can affect vitamin metabolism and absorption, although how alcohol impairs such biochemical pathways remains to be elucidated. • For this purpose, we designed INTERACTOMES and employed transcriptomic data analysis approaches to study the neural tissue of Mus musculus exposed to ethanol prenatally and postnatally, simulating conditions that could lead to FAS development at different life stages. MOLECULAR MECHANISMS FOR GROWTH SUPPRESSION
  15. 15. This showed that FAS can promote early changes in neurotransmitter release and glutamate equilibrium, as well as an abnormal calcium influx that can lead to neuroinflammation and impaired neurodifferentiation, both extensively connected with vitamin action and metabolism. Genes related to retinoic acid, niacin, vitamin D, and folate metabolism were under expressed during neurodevelopment and appear to contribute to neuroinflammation progression and impaired synapsis.
  16. 16. Alcohol increased embryonic and decidual ADNP expression at 24 hours and it persisted in the embryo for 10 days Because ADNP is a neuro-protectant, these findings suggest that it may be released as a protective mechanism in FAS Peptides NAPVSIPQ (NAP) and SALLRSIPA (SAL), related to activity dependent neuro-protective protein (ADNP) prevent alcohol induced damage in a mouse model of FAS
  17. 17. Advances in development of novel anti-oxidant therapies as an approach for fetal alcohol syndrome prevention Currently, there is no known effective strategy for prevention (other than alcohol avoidance) or treatment. The use of antioxidants as a potential therapeutic strategy for the treatment using whole-embryo and culture cells models of FASD was performed. The induction of oxidative stress is believed to be one central process linked to the development of the disease. This experiment concluded that the imbalance of the intracellular redox state contributes to the pathogenesis observed in FASD models, and we suggest that antioxidant therapy can be considered a new efficient strategy to mitigate the effects of prenatal ethanol exposure.
  18. 18. A common molecular vulnerability in autism and fetal alcohol spectrum disorder was found Both disorders have symptoms of social impairment and originate during brain development in utero A NORTHWESTERN MEDICINE STUDY
  19. 19. RAT MOTHER ( FED WITH ALCOHOL DURING PREGNANCY ) MALE OFFSPRING FEMALE OFFSPRING SHOWED SOCIAL IMPAIRMENT AND ALTERED LEVELS OF AUTISM- RELATED GENES FOUND IN HUMANS WERE NOT AFFECTED
  20. 20. This leads to apoptosis of the CRANIAL NEURAL CREST CELLS (CNCCs) via two known mechanisms. Ethanol can activate G-protein coupled receptors, activating phospholipase C, which breaks down IP2 to IP3 and DAG. IP3 mediated release of intracellular calcium stores leads to increased Ca+2 dependent kinase activation. Calmodulin and CamKII activation leads to phosphorylation and proteolysis of β-catenin, which affects gene expression and CNCC apoptosis. Reducing β-catenin degradation is a potential therapeutic target, and kinase inhibitors for CamKII and GSK3β (canonical Wnt inhibitor) have been tested. ETHANOL EXPOSURE CAN INDUCE THE CASPASE CASCADE ETHANOL-INDUCED PRODUCTION OF CERAMIDE FROM SPHINGOMYELIN is another potential mechanism that leads to the malfunction of folbp-1, folate binding protein-1, and contributing to FA deficiency. This can lead to increased CNCC death. Supplementation with FA can potentially rescue CNCC death. Dotted line indicates possible interaction between canonical and noncanonical Wnt signaling pathways
  21. 21. INDIAN COUNTRY HAS LED RESPONSE TO THIS ISSUE BY DEVELOPING THE MAJORITY OF PREVENTION AND INTERVENTION CIRRCULA THE NORTHWEST TRIBAL FASD PROJECT SEEKS TO REDUCE THE INCIDENCE OF FASD AND TO ASSIST TRIBAL COMMUNITIES TO IMPROVE THE QUALITY OF LIFE OF THOSE LIVING WITH FASD WE MUST ALSO PROMOTE HOLISTIC HEALING THROUGH TRADITIONAL AND DEVELOPMENTALLY APPROPRIATE TECHNIQUES THAT ADDRESS THE PHYSICAL, INTELLECTUAL, EMOTIONAL AND SPIRITUAL NEEDS OF INDIVIDUALS AFFECTED BY FASD STEPS TAKEN IN INDIA
  22. 22. CONCLUSIONS: Until the advent of effective prevention measures, it will remain necessary to seek ways to treat the life-long neurobehavioral consequences of prenatal alcohol exposure.
  23. 23. THANK YOU QUERIES PLEASE !!!

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